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      • Experimental study of reversal of multidrug resistance in human leukemia K562/DOX cells by toad venom

        Hu, Pei,Qiu, Zhichao,Li, Yaohe,Liu, Anping,Chen, Zhixiong,Huliwen, Huliwen,Luo, Man,Guxuekui, Guxuekui,Xiaoyang, Xiaoyang,Xie, Ying,Lan, Hai Techno-Press 2021 Advances in nano research Vol.11 No.2

        Acute leukemia is a malignant tumor originating from the hematopoietic system with the highest incidence and mortality. At present, the main clinical treatment of leukemia is still chemotherapy, during the course of which the multidrug resistance (MDR) will significantly reduce remission rate and disease-free survival rate of patients. MDR is the most important factor affecting refractory/recurrent acute leukemia. Therefore, reversing leukemia MDR is one of the best ways to improve the complete remission rate of refractory/recurrent acute leukemia, and the study of drugs and methods to overcome leukemia MDR has received extensive attention in the leukemia research field. This study was to primarily investigate the effects of Liushen pills on leukemia drug-resistant cell line K562/DOX in inhibiting growth, reversing resistance and inducing apoptosis in anticipation of providing useful cytological and molecular biological basis for the treatment of refractory/recurrent acute leukemia. The serum containing toad venom was prepared by means of Chinese drug serum pharmacology. MTT assay was used to detect the inhibitory rates of human leukemia cell line K562/DOX after being treated with the serum containing toad venom as well as daunorubicin, or with the serum containing toad venom alone at different time points. Real-time fluorescent quantitative analysis (RT-PCR) was performed to determine the effects of serum containing toad venom on the expression of BCL-2 mRNA in human leukemia cell line K562/DOX. Compared to the control group, toad venom showed inhibitory effects on K562/DOX cells; the expression level of BCL-2 mRNA in toad venom group were decreased, indicating that toad venom may reverse the resistance of K562/DOX cells by down-regulating the expression level of MDR1.

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